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Although a number of patients with anorexia nervosa— especially adolescents with relatively recent onset of the disorder—experiencemarked improvement andevenremission after treatment, toomanypatientsdonot. Anorexia nervosa is characterized by low weight due to persistent efforts to restrict energy intake, often through the consumption of lowfat, low-calorie foods (1). There is no U.S. Food and Drug Administration–approved medication for anorexia nervosa, and no medication has demonstrated substantial efficacy for both weight regain and the psychological symptoms of anorexia nervosa. Although it is more difficult to assess the absolute efficacy of nonpharmacological treatments for anorexia nervosa (e.g., nutritional rehabilitation in more intensive settings and/or psychotherapies), recent high-quality clinical trials comparing treatments make it clear that the majority of patients, especially adults, do notmeet criteria for remission or recovery after treatment (2). Given the need for more efficacious interventions, repeated calls have been made to develop treatments targeting anorexia nervosa–specific mechanisms (3), which would require an improved understanding of those mechanisms. In this issue of the Journal, Kaye and colleagues advance this important inquiry by probing mechanisms related to the response to gustatory stimuli in varying metabolic states (4). In healthy individuals, metabolic state modulates the reward salience of food in an adaptive fashion: fasting potentiates its subjective (reward) value, whereas satiation attenuates it. Kaye et al. used functional MRI to investigate whether this adaptive pattern is altered in women with remitted anorexia nervosa. Specifically, the authors examined how fed and fasted conditions affect blood-oxygen-level-dependent (BOLD) activation and functional connectivity in response to two tastants in women with remitted anorexia nervosa compared to women without a history of the disorder. Contrary to the expectation that the two tastants (a sucrose solution and ionic water) would exhibit different neural responses across conditions and groups, the pattern of results was similar for the two tastants. For both tastants together, two clusters within prespecified tasteand reward-related brain regions showed group differences in the pattern of activation across the fed and fasted conditions. In comparison women, the fasted condition was associated with a greater tastant-related increase in BOLD signal in two ventral caudal putamen clusters, consistent with adaptive potentiation of food reward when metabolic needs are more pressing. In women with remitted anorexia nervosa, the pattern was reversed, with the fed condition associated with the greater increase in BOLD signal in these two clusters. This opposing pattern of activation was also observed for tastant-related connectivity in one of the ventral caudal putamen clusters: in comparison women, this cluster had more positive correlations with seed regions in the right dorsal mid insula and the right ventral caudal putamen in the fasted condition versus the fed condition, whereas in womenwith remitted anorexia nervosa, these correlations were more positive in the fed condition. When looking at each condition separately, group differences were found for the fasted but not the fed condition: in the fasted condition,womenwith remitted anorexia nervosa were generally characterized by lower activation andlesspositivefunctional connectivity in response to tastants in the striatal regions. Interestingly, despite the groups’ opposing neural patterns across metabolic conditions, they reportedhighly similar subjective experiences of hunger and tastant pleasantness across the two conditions. In summary, despite similar ratings of hunger and tastant pleasantness in women with remitted anorexia nervosa, findings within the prespecified tasteand reward-related regions suggest smaller increases in tastant-related activation, and reduced tastant-related positive functional connectivity, in the fasted state for women with remitted anorexia nervosa. The authors suggest that the “reduced recruitment of the striatal aspects of this circuitry in response to tastants when hungry” may result in impaired “translation of taste reward value to motivated eating behavior,” representing a potential neural explanation for the persistent dietary restriction observed in anorexia nervosa. [This study] addresses many of the challenges involved in advancing our understanding of the mechanisms underlying persistent dietary restriction in anorexia nervosa.

Neural Insensitivity to the Effects of Hunger: A Potential Mechanism Underlying Persistent Dietary Restriction in Anorexia Nervosa?